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Single protein drives growth and spread of deadliest cancer, research shows

Scientists may have found the key to tackling an especially lethal pancreatic cancer sub-type.
Scientists may have found the key to tackling an especially lethal pancreatic cancer sub-type. Scientists may have found the key to tackling an especially lethal pancreatic cancer sub-type.

Addiction to a single protein could hold the key to taming one of the world’s deadliest cancers, research suggests.

Scientists have discovered that a particularly aggressive sub-type of pancreatic cancer needs the molecule to grow and spread.

They are now looking at ways of suppressing the protein, TP63, to increase the survival chances of patients with the disease.

Pancreatic cancer, which affects almost 10,000 people each year in the UK, has a bad reputation as one of the most lethal cancers.

On average, a patient with pancreatic cancer will survive only about two years after diagnosis.

But some individuals with an especially aggressive sub-type of the disease often succumb even earlier, after less than a year.

US researchers investigating this super-deadly pancreatic cancer sub-type found that the gene for TP63 was uniquely active in its tumour cells.

Writing in the journal Cell Reports, they point out that the molecule does not belong in pancreas cells.

P63 normally plays a role in the production of squamous cells, long thin cells required for skin formation.

But in pancreatic tumours, the cancer version of the protein – TP63 – fuelled out-of-control growth and helped the disease spread around the body.

The good news was that the cancer seemed to depend on the molecule for its on-going survival, raising hopes of developing targeted treatments.

Lead scientist Dr Timothy Somerville, from Cold Spring Harbour Laboratory in New York, said: “The cancer cells become so reliant on P63 that they actually require P63 for their continued growth.

“So moving forward, we’re looking into approaches to suppress inappropriate P63 activity as a treatment option for patients.”

Another goal for the team is to discover why the gene becomes active in the pancreas in the first place.

“If we can stop it from ever happening, it could be really good for the survival of this most vulnerable group of cancer patients,” said Dr Somerville.